Autism spectrum disorders may be due to cerebral toxoplasmosis associated with chronic neuroinflammation causing persistent hypercytokinemia that resulted in an increased lipid peroxidation, oxidative stress, and depressed metabolism of endogenous and exogenous substances

Prandota, J

doi:10.1016/j.rasd.2009.09.011

Cited by 44 publications

(27 citation statements)

References 496 publications

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“…In a mouse model system, T. gondii infection was found to generate sensorimotor deficits in animals without major brain damage or cognitive dysfunction (Gulinello et al, 2010). In addition to these links of T. gondii to schizophrenia, Parkinson's disease and OCD, T. gondii has been associated with Tourette's syndrome (P<0.07) (Krause et al, 2010) and a link with autism spectrum disorders has been speculated (Prandota, 2010). It is intriguing that dysregulation of dopamine has been implicated in all these disorders.…”

Section: Toxoplasma and Neurological Disordersmentioning

confidence: 99%

Toxoplasma gondii infection and behaviour – location, location, location?

McConkey

Martin

Bristow

et al. 2013

Journal of Experimental Biology

193

156

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SummaryParasite location has been proposed as an important factor in the behavioural changes observed in rodents infected with the protozoan Toxoplasma gondii. During the chronic stages of infection, encysted parasites are found in the brain but it remains unclear whether the parasite has tropism for specific brain regions. Parasite tissue cysts are found in all brain areas with some, but not all, prior studies reporting higher numbers located in the amygdala and frontal cortex. A stochastic process of parasite location does not, however, seem to explain the distinct and often subtle changes observed in rodent behaviour. One factor that could contribute to the specific changes is increased dopamine production by T. gondii. Recently, it was found that cells encysted with parasites in the brains of experimentally infected rodents have high levels of dopamine and that the parasite encodes a tyrosine hydroxylase, the rate-limiting enzyme in the synthesis of this neurotransmitter. A mechanism is proposed that could explain the behaviour changes due to parasite regulation of dopamine. This could have important implications for T. gondii infections in humans.

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Section: Toxoplasma and Neurological Disordersmentioning

confidence: 99%

Toxoplasma gondii infection and behaviour – location, location, location?

McConkey

Martin

Bristow

et al. 2013

Journal of Experimental Biology

193

156

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“…In vitro preincubation of tachyzoites with recombinant human prolactin resulted in a significant reduction (up to 36.15%) in replication abilities of the parasite, and the inhibition of replication was caused by a limited capacity of the parasites to penetrate host's cells as demonstrated by the reduced number of infected cells [212]. More detailed effects of chronic T. gondii infection concerning modulation of human innate immunity and metabolism were presented in other works [213][214][215][216]. Tables 9 and 10 summarized host cell-mediated evasion strategy against infection with the parasite.…”

Section: Humansmentioning

confidence: 99%

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Pr¹,

ota²

2013

J Diabetes Metab

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Recently, it was suggested that maternal T and potentially B cells transferred during pregnancy and/or the breast milk feeding and their encounter with the antigen in mesenteric lymph nodes might play a role in development of type 1 diabetes mellitus (T1DM). T. gondii infection during gestation and/or after birth may be responsible for development of both T1DM and T2DM in children, adolescents and adults because: a) maternal microchimerism in peripheral blood was demonstrated to be significantly higher in patients with T1DM compared to unaffected siblings and healthy subjects, b) transmission of T. gondii as a Trojan horse in various types of eukaryotic cells, including T and B lymphocytes, c) swallowing by the fetus of amniotic fluid containing infected leukocytes and other cells, d) elimination of T. gondii in the breast milk during lactation, e) involvement of mesenteric lymph nodes after oral infection with the parasite, and f) damage of the myenteric neurons during infection with the parasite in both the animals with streptozotocin-induced diabetes and diabetic patients. Moreover, a significantly lower occurrence of antibodies against T. gondii found in the sera of patients with T1DM compared with their first-degree family members or healthy controls may be due to their T and/or B cell exhaustion perspective caused by chronic infection with the parasite. This suggestion may be supported by the finding that latent toxoplasmosis was associated with markedly reduced lymphocyte B-cell counts responsible for production of antibodies, markedly lower serum IgG, IgM, and IgA levels, and a significant suppression of IL-2. On the other hand, patients with T2DM had increased anti-T. gondii antibodies significantly more frequently than respective controls. Impaired vascular endothelial function characteristic for the patients with diabetes mellitus may be at least in part due to the preferential T. gondii infection of endothelial cells. Vitamin D and minocycline exerted beneficial effects on development and clinical course of diabetes mellitus probably because of their immunomodulatory and antitoxoplasmatic activities. These data strongly suggest that the parasite play an important role in development of both types of diabetes mellitus.

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“…Neonatal exposure to inflammation has been extensively studied in the context of neuropsychological disorders (Angelidou et al 2012;Ashwood et al 2006;Garay et al 2012;Prandota 2010). When disrupted by the introduction of the H1N1 strain of human influenza virus at various stages of prenatal development, genetic, brain structure, behavioral, and neurochemical abnormalities were subsequently seen in the affected mice progeny (Fatemi 2009).…”

Section: Animal Analogues For Human Subjects With Asdmentioning

confidence: 99%

Exploring the Potential Role of Inflammation as an Etiological Process in ASD

Elias

Sullivan

Lee

et al. 2015

Rev J Autism Dev Disord

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The heterogeneity in the behavioral presentation of autism spectrum disorder (ASD) may be surpassed only by the level of heterogeneity in its etiology. There are diverse pathways to the singular diagnostic outcome of ASD, and several etiological risk factors have been proposed in recent years. This review paper examines the role of inflammation as one possible etiologic factor in ASD, juxtaposed in the context of research on the role of inflammation in other psychiatric disorders. Human, animal, and postmortem studies of inflammation in ASD were surveyed, and their direct and indirect contributions to developing potential inflammation-based treatments, as well as potential preventative considerations, in ASD were reviewed. Although the mechanisms that link inflammation and ASD remain unknown, there exists a sizable multidisciplinary literature suggesting inflammation as a trans-etiological process.

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Autism spectrum disorders may be due to cerebral toxoplasmosis associated with chronic neuroinflammation causing persistent hypercytokinemia that resulted in an increased lipid peroxidation, oxidative stress, and depressed metabolism of endogenous and exogenous substances

Cited by 44 publications

References 496 publications

Toxoplasma gondii infection and behaviour – location, location, location?

Toxoplasma gondii infection and behaviour – location, location, location?

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Exploring the Potential Role of Inflammation as an Etiological Process in ASD

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